Solar cycle dependence of the seasonal variation of auroral hemispheric power

Although much has been done on the hemispheric asymmetry (or seasonal variations) of auroral hemispheric power (HP), the dependence of HP hemispheric asymmetry on solar cycle has not yet been studied. We have analyzed data during 1979–2010 and investigated the dependence of HP hemispheric asymmetry/seasonal variation for the whole solar cycle. Here we show that (1) the hemispheric asymmetry of HP is positively correlated to the value of solar F10.7 with some time delay; (2) it is closely related to the coupling function between the solar wind and magnetosphere; and (3) the winter hemisphere receives more auroral power than the summer hemisphere for K _p～0 to 6. The statistic results can be partly understood in the framework of the ionospheric conductivity feedback model. The similarity and differences between our results and previous results are discussed in the paper.     

Mutant antimicrobial peptide hepcidin is associated with severe juvenile hemochromatosis

Animal models indicate that the antimicrobial peptide hepcidin (HAMP; OMIM 606464) is probably a key regulator of iron absorption in mammals. Here we report the identification of two mutations (93delG and 166C-->T) in HAMP on 19q13 in two families with a new type of juvenile hemochromatosis.     

Reflection signature of seismic and aseismic slip on the northern Cascadia subduction interface

At the northern Cascadia margin, the Juan de Fuca plate is underthrusting North America at about 45 mm x yr(-1) (ref. 1), resulting in the potential for destructive great earthquakes. The downdip extent of coupling between the two plates is difficult to determine because the most recent such earthquake (thought to have been in 1700) occurred before instrumental recording. Thermal and deformation studies indicate that, off southern Vancouver Island, the interplate interface is presently fully locked for a distance of approximately 60 km downdip from the deformation front. Great thrust earthquakes on this section of the interface (with magnitudes of up to 9) have been estimated to occur at an average interval of about 590 yr (ref. 3). Further downdip there is a transition from fully locked behaviour to aseismic sliding (where high temperatures allow ductile deformation), with the deep aseismic zone exhibiting slow-slip thrust events. Here we show that there is a change in the reflection character on seismic images from a thin sharp reflection where the subduction thrust is inferred to be locked, to a broad reflection band at greater depth where aseismic slip is thought to be occurring. This change in reflection character may provide a new technique to map the landward extent of rupture in great earthquakes and improve the characterization of seismic hazards in subduction zones.     

Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS

Natural killer (NK) cells provide defense in the early stages of the innate immune response against viral infections by producing cytokines and causing cytotoxicity. The killer immunoglobulin-like receptors (KIRs) on NK cells regulate the inhibition and activation of NK-cell responses through recognition of human leukocyte antigen (HLA) class I molecules on target cells KIR and HLA loci are both highly polymorphic, and some HLA class I products bind and trigger cell-surface receptors specified by KIR genes. Here we report that the activating KIR allele KIR3DS1, in combination with HLA-B alleles that encode molecules with isoleucine at position 80 (HLA-B Bw4-80Ile), is associated with delayed progression to AIDS in individuals infected with human immunodeficiency virus type 1 (HIV-1). In the absence of KIR3DS1, the HLA-B Bw4-80Ile allele was not associated with any of the AIDS outcomes measured. By contrast, in the absence of HLA-B Bw4-80Ile alleles, KIR3DS1 was significantly associated with more rapid progression to AIDS. These observations are strongly suggestive of a model involving an epistatic interaction between the two loci. The strongest synergistic effect of these loci was on progression to depletion of CD4(+) T cells, which suggests that a protective response of NK cells involving KIR3DS1 and its HLA class I ligands begins soon after HIV-1 infection.     

The K-Cl cotransporter KCC3 is mutant in a severe peripheral neuropathy associated with agenesis of the corpus callosum

Peripheral neuropathy associated with agenesis of the corpus callosum (ACCPN) is a severe sensorimotor neuropathy associated with mental retardation, dysmorphic features and complete or partial agenesis of the corpus callosum. ACCPN is transmitted in an autosomal recessive fashion and is found at a high frequency in the province of Quebec, Canada. ACCPN has been previously mapped to chromosome 15q. The gene SLC12A6 (solute carrier family 12, member 6), which encodes the K+-Cl- transporter KCC3 and maps within the ACCPN candidate region, was screened for mutations in individuals with ACCPN. Four distinct protein-truncating mutations were found: two in the French Canadian population and two in non-French Canadian families. The functional consequence of the predominant French Canadian mutation (2436delG, Thr813fsX813) was examined by heterologous expression of wildtype and mutant KCC3 in Xenopus laevis oocytes; the truncated mutant is appropriately glycosylated and expressed at the cellular membrane, where it is non-functional. Mice generated with a targeted deletion of Slc12a6 have a locomotor deficit, peripheral neuropathy and a sensorimotor gating deficit, similar to the human disease. Our findings identify mutations in SLC12A6 as the genetic lesion underlying ACCPN and suggest a critical role for SLC12A6 in the development and maintenance of the nervous system.